OBJECTIVE: To study the relationship between the different replication status of hepatitis B virus (HBV) and mutations in the core promoter (CP) in mother and her child infected by mother-to-infant transmission.
METHODS: The core promoter was amplified by PCR and cloned into pGEM-T vector with the T-A cloning technique. The recombinant plasmid pGEM-CP was confirmed by digestion with restriction enzyme Apa Ⅰ and Sac Ⅰ. Two clones were selected to be sequenced in each patient.
RESULTS: Every pair of mother and child had same serotype and genotype and the homology of nucleotides encoding “a” determinant was 98%-100%. The number of mutations in the core promoter of patients with a high replication status was less than that in those with a low replication status. Mutations were mainly distributed in basia core promoter (BCP) and the inhibitor region of Kunitz-type serine protease. This difference was not associated with mother or child.
CONCLUSION: The different replication status of HBV is caused by mutations in the core promoter in mother and child infected by mother-to-infant transmission and appears to be not associated with the status of development of the infection.